Gene expression profile of Cnot3(+/+) & Cnot3 (∆/∆) pro-B cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE87635 | GEO | 2016/11/21
SECONDARY ACCESSION(S): PRJNA345465
REPOSITORIES: GEO
Similar Datasets
Project description:The CCR4-NOT complex, bearing poly(A) deadenylation activity, is a highly conserved regulator that is involved in biological control; however its action mechanisms and physiological targets remain unclear. Using genetic deletion of the CNOT3 subunit of this complex in early B cell progenitors, we show that CNOT3 plays a critical role in pro- to pre-B cell transition. CNOT3 participated in controlling germline transcription, compaction of the immunoglobulin heavy chain (Igh) locus, and Igh rearrangement, and in destabilizing tumor suppressor p53 mRNA. Moreover, by genetic ablation of p53 or introduction of pre-rearranged Igh transgene, the B cell developmental defect in the Cnot3 knockout background could be partly rescued, suggesting that CCR4-NOT complex exerts critical control in B cell differentiation processes by co-utilizing transcriptional and post-transcriptional mechanisms. Pro-B cells mRNA profiles of Mb1(cre/+) and Cnot3(fl/fl)Mb1(cre/+) mice were generated by deep sequencing using Illumina HiSeq 1500
2015-07-23 | E-GEOD-64455 | biostudies-arrayexpress
Project description:EBF1 interacts with CNOT3 and histidine 240 of EBF1 is a critical residue for this interaction. We studied H240 dependent EBF1 occupancy and gene expression regulation by genome-wide ChIP and microarray analysis. We also performed RNASeq analysis in pro-B cells to study the role of Cnot3 in early B cells development. This SuperSeries is composed of the SubSeries listed below.
2016-11-21 | GSE87637 | GEO
Project description:This goal of this study was to identify genes that are deregulated in the absence of EZH2 in early lymphocyte progenitors. Due to a requirement for EZH2 to repress Cdkn2a in early B and T cell development we generated Cdkn2a-/-Ezh2fl/fl Il7racre/+ mice. We examined gene expression by RNA-sequencing in sorted pro-B cells (B220+CD19+CD43+), DN3 cells (Lin- CD25+ CD117-), from Cdkn2a-/- Ezh2fl/fl Il7racre/+ and Cdkn2a-/- Il7racre/+ control mice. Reads were aligned to the mm10 reference genome by Tophat2.1.0. Reads were assigned to genes using the htseq-count tool from HTSeq v 0.6.1 and gene annotations from Ensembl release 78. Differential expression was calculated across 3 independent replicates by EdgeR. We found that pro-B and DN3 cells remain specified to their respective lineages despite loss of EZH2. In contrast, loss of EZH2 led to expression of alternate lineage determinants in pro-B but not DN3 cells indicating that EZH2 is required for lineage commitment in B, but not T lymphocyte progenitors.
2020-01-29 | GSE133993 | GEO
Project description:We identified that IL-33 is expressed in pro-B (B220+ IgM- CD19+ CD43+) and large pre-B cells (B220+ IgM- CD19+ CD43- FSC-Ahi SSC-Ahi) in mice. We assessed for IL-33-dependent gene expression differences in these B cell stages by performing bulk RNA-sequencing of FACS-purified pro-B and large pre-B cells from WT and IL-33-deficient 8 week old adult, naive female mice.
2019-07-04 | GSE132123 | GEO
Project description:We used the NanoString mouse nCounter miRNA expression platform to compare the miRNA expression profiles of pro-B cells sorted from fetal liver and adult bone marrow in order to gain insight into changes in miRNA expression during B cell ontogeny. Fetal liver and adult bone marrow cells were harvested and FACS sorted for pro-B cells (B220+CD43+IgM-veCD19+CD24+). Total RNA was extracted and used for sample preparation and hybridization per manufacturer's instructions.
2012-02-17 | E-GEOD-35107 | biostudies-arrayexpress
Project description:The CCR4-NOT complex, bearing poly(A) deadenylation activity, is a highly conserved regulator that is involved in biological control; however its action mechanisms and physiological targets remain unclear. Using genetic deletion of the CNOT3 subunit of this complex in early B cell progenitors, we show that CNOT3 plays a critical role in pro- to pre-B cell transition. CNOT3 participated in controlling germline transcription, compaction of the immunoglobulin heavy chain (Igh) locus, and Igh rearrangement, and in destabilizing tumor suppressor p53 mRNA. Moreover, by genetic ablation of p53 or introduction of pre-rearranged Igh transgene, the B cell developmental defect in the Cnot3 knockout background could be partly rescued, suggesting that CCR4-NOT complex exerts critical control in B cell differentiation processes by co-utilizing transcriptional and post-transcriptional mechanisms.
2015-07-23 | GSE64455 | GEO
Project description:Through RNA immunoprecipitation with anti-Cnot3 antiboy from mouse heart lysates and RNA-seq (Cnot3 RIP-seq) and gene ontology analyses, we show the comprehensive picute of cardiac Cnot3 target genes.
2018-08-31 | GSE103629 | GEO
Project description:Using cultured pro-B cells from mice carrying two Ebf1 alleles flanked with loxP sites and an inducible Cre recombinase, target genes of Ebf 1 and the effect of Ebf1 deletion on the cells was analyzed Ebf1 fl/fl pro-B cells and heterozygote control cells were treated with 4-hydroxy-tamoxifen (4OHT) for 24 h to activate an ER-Cre fusion protein. Four days after treatment no Ebf1 expression could by detected and RNA was extracted for expression analysis.
2010-07-29 | E-GEOD-21454 | biostudies-arrayexpress
Project description:Decay of mRNAs initiates with shortening of the poly(A) tail. Although the CCR4-NOT complex participates in deadenylation, how it becomes activates remain obscure. We show that complete deficiency in CNOT3, subunit 3 of this complex, is lethal in mice, but that heterozygotes survive as lean mice with hepatic and adipose tissues containing reduced lipid levels. Cnot3+/- mice have enhanced metabolic rates and remain lean on high-fat diets. To examine the underlying mechanisms by which CNOT3 is involved in the control of metabolic balance, we compared the gene expression profiles of wild-type and Cnot3+/- mice using Affymetrix microarray technology. We chose to analyze the liver because the CNOT3 level in the liver was affected by the feeding condition and because the liver plays a major role in glucose and lipid metabolism.
2011-12-09 | GSE18924 | GEO
Project description:Decay of mRNAs initiates with shortening of the poly(A) tail. Although the CCR4-NOT complex participates in deadenylation, how it becomes activates remain obscure. We show that complete deficiency in CNOT3, subunit 3 of this complex, is lethal in mice, but that heterozygotes survive as lean mice with hepatic and adipose tissues containing reduced lipid levels. Cnot3+/- mice have enhanced metabolic rates and remain lean on high-fat diets. To examine the underlying mechanisms by which CNOT3 is involved in the control of metabolic balance, we compared the gene expression profiles of wild-type and Cnot3+/- mice using Affymetrix microarray technology. We chose to analyze the liver because the CNOT3 level in the liver was affected by the feeding condition and because the liver plays a major role in glucose and lipid metabolism. The livers were isolated from 12-week-old wild-type and Cnot3+/- mice (n = 2 for each genotype).
2011-12-09 | E-GEOD-18924 | biostudies-arrayexpress